What is eczema?
Atopic dermatitis, also called eczema, is a common skin condition. "Atopic" refers to a heightened sensitivity toward allergens, leading to frequent, excessive immune reactions that inflame and irritate the skin (dermatitis). Other atopic diseases include allergic rhinitis and asthma. It is most common during childhood, with a prevalence of up to 25% of children affected, but can persist into adulthood; over a lifetime, 7–10% of people will get eczema at some point.[1]
What are the main signs and symptoms of eczema?
Red, inflamed skin lesions that can occur on many parts of the body. These lesions are dry and often itchy, swollen, oozing, crusting, and with time can become lichenified (thick and leathery). Scratching is common, which leads to a vicious cycle of irritation leading to scratching leading to further irritation. Psychological symptoms such as depression, anxiety, and insomnia are also common.
How is eczema diagnosed?
Diagnosis is generally based on signs/symptoms and medical history. Eczema is chronic, so it can take a while to be sure that the lesions are due to eczema rather than a more acute phenomenon like an infection, an acute or transient allergic reaction, or exposure to harmful chemicals. A history or family history of asthma, hay fever, and dry skin also makes eczema more likely. To determine the severity of atopic dermatitis and track treatment progress, researchers and doctors objectively measure several characteristics of the lesions with scoring systems such as EASI and SCORAD.[2]
What are some of the main medical treatments for eczema?
The use of topical barrier creams and topical corticosteroids, such as hydrocortisone, are typically the first line of treatment. Oral and topical antihistamines are also commonly used early. If this proves insufficient, immunosuppressive (focused on curtailing the excessive immune system activation) drugs are frequently employed. Some such drugs and drug types include monoclonal antibodies, JAK inhibitors, steroids, calcineurin inhibitors, methotrexate, mycophenolate mofetil, and cromoglycate. Phosphodiesterase inhibitors are also sometimes used to induce vasodilation.
Have any supplements been studied for eczema?
Several supplements have and continue to be investigated for eczema, though at present, the only ones approaching credibility from clinical trials are vitamin D[3] and probiotics.[4] They are also mechanistically plausible. Vitamin D is known to help regulate the immune system and plays a role in the formation of filaggrin, which helps to maintain the skin's moisture barrier. Some probiotics play a significant role in regulating the immune system to reduce excessive inflammation, maintain the gut barrier and prevent further inflammation.
How could diet affect eczema?
Are there any other treatments for eczema?
Fabric selection may play a meaningful part in reducing itching. Fabrics with scratchier fibers and wider spaces between fibers, such as wool, are worse, whereas cotton, silk, and ultrafine wool may be better choices.[7] There is also interest in a number of alternative fabrics treated with antibacterial agents, such as silver, zinc oxide, and borage oil, with some clinical evidence in particular for silver, though more research is needed.[8] Phototherapy with narrow-band UV-B and UV-A1 has also seen a considerable amount of research and is likely effective for reducing the severity of eczema.[9]
What causes eczema?
Genetics plays a considerable role, and a number of mechanistically plausible genes have been linked to eczema risk.[10] Additionally, microbiome disruption is highly common in eczema, and with the vital role in immune regulation that the microbiome plays, this is plausible.[11] Other possible factors include smoking, maternal alcohol consumption and stress/anxiety, being born in winter, phthalate exposure, and hard water. The early-life use of antibiotics[12] and acetaminophen are also associated with eczema, though it's possible that this is due to a dysfunctional immune system leading both to the need for those medications as well as eczema.
Examine Database: Eczema (Atopic Dermatitis)
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Frequently asked questions
Atopic dermatitis, also called eczema, is a common skin condition. "Atopic" refers to a heightened sensitivity toward allergens, leading to frequent, excessive immune reactions that inflame and irritate the skin (dermatitis). Other atopic diseases include allergic rhinitis and asthma. It is most common during childhood, with a prevalence of up to 25% of children affected, but can persist into adulthood; over a lifetime, 7–10% of people will get eczema at some point.[1]
Red, inflamed skin lesions that can occur on many parts of the body. These lesions are dry and often itchy, swollen, oozing, crusting, and with time can become lichenified (thick and leathery). Scratching is common, which leads to a vicious cycle of irritation leading to scratching leading to further irritation. Psychological symptoms such as depression, anxiety, and insomnia are also common.
Diagnosis is generally based on signs/symptoms and medical history. Eczema is chronic, so it can take a while to be sure that the lesions are due to eczema rather than a more acute phenomenon like an infection, an acute or transient allergic reaction, or exposure to harmful chemicals. A history or family history of asthma, hay fever, and dry skin also makes eczema more likely. To determine the severity of atopic dermatitis and track treatment progress, researchers and doctors objectively measure several characteristics of the lesions with scoring systems such as EASI and SCORAD.[2]
The SCORAD index is an evaluation tool for the severity of atopic dermatitis that combines information on the extent, intensity, and subjective symptoms of the disease. To determine extent, the sites affected by eczema are shaded on a drawing of a body to calculate the affected area (A) as a percentage of the whole body, which has a maximum possible score of 100%. For intensity (B), a representative area is selected and six signs of inflammation (redness, swelling, itching, dryness, skin thickening, and oozing/crusting) are assessed on a three-point scale, giving a maximum score of 18 points. Subjective symptoms (C) include itchiness and sleeplessness, both of which are rated on a 10-point scale and combined for a maximum score of 20 points. The SCORAD for an individual is calculated as A/5 + 7B/2 + C, and therefore a maximum score is 103 points.
The use of topical barrier creams and topical corticosteroids, such as hydrocortisone, are typically the first line of treatment. Oral and topical antihistamines are also commonly used early. If this proves insufficient, immunosuppressive (focused on curtailing the excessive immune system activation) drugs are frequently employed. Some such drugs and drug types include monoclonal antibodies, JAK inhibitors, steroids, calcineurin inhibitors, methotrexate, mycophenolate mofetil, and cromoglycate. Phosphodiesterase inhibitors are also sometimes used to induce vasodilation.
Several supplements have and continue to be investigated for eczema, though at present, the only ones approaching credibility from clinical trials are vitamin D[3] and probiotics.[4] They are also mechanistically plausible. Vitamin D is known to help regulate the immune system and plays a role in the formation of filaggrin, which helps to maintain the skin's moisture barrier. Some probiotics play a significant role in regulating the immune system to reduce excessive inflammation, maintain the gut barrier and prevent further inflammation.
So far, vitamin D is the only essential nutrient that has convincing evidence for improving atopic dermatitis. In a meta-analysis, 4 trials found evidence for a meaningfully beneficial effect.[3] Two used 1,600 IU; one used 1,000 IU; and one used sun exposure in a subtropical climate. Two were in children, and two were in older populations. More high-quality research is needed to confirm these findings and determine the best scenarios for using vitamin D for atopic dermatitis.
Other nutrients have been lightly researched, but they’re not worth mentioning at present.
Probiotics and synbiotics One meta-analysis of randomized trials in children found evidence of a beneficial effect for participants in the ages 1–18 category, but the effect on participants younger than 1 wasn’t statistically significant or as large.[4] In particular, the most evidence for a positive outcome was found for mixtures of probiotics. However, the studies in general had a notable risk for bias, so more research will be needed to both confirm efficacy and clarify which combinations of probiotics are best. The meta-analysis only included studies where a dermatologist had evaluated the participants with the SCORAD method, which lends itself to a higher level of objective measurements but limited the number of studies. Another meta-analysis that included any trial that used probiotics to treat pediatric eczema found a general benefit, but again, multiple studies on particular strains or mixtures are needed before we can know how to optimally use probiotics. Finally, a meta-analysis looked at synbiotic (a combination of pre- and probiotics) supplements, and out of 6, a statistically significant benefit was found, but it’s unclear if synbiotics are superior to probiotics or which synbiotics are best.[38]
Pharmaceutical and supplement therapies for atopic dermatitis are largely centered around substances that modify immune response to reduce the effects of persistent inflammation.
The use of partially hydrolyzed whey protein infant formula may reduce the risk of eczema later in life.[5] In addition, sufficient levels of vitamin-d, zinc, and selenium are associated with a lower risk of eczema, though besides vitamin D, it's not clear if they are causally linked.[6]
About one-third of children with eczema have a food allergy, and eating certain foods will make their symptoms of eczema worse. Some of the most common food allergies include cow’s milk, hen’s eggs, peanut, soy, nuts, and fish.[13] Interestingly, there is little evidence that exclusion diets have any benefit for adults and children with eczema.[14]
Fabric selection may play a meaningful part in reducing itching. Fabrics with scratchier fibers and wider spaces between fibers, such as wool, are worse, whereas cotton, silk, and ultrafine wool may be better choices.[7] There is also interest in a number of alternative fabrics treated with antibacterial agents, such as silver, zinc oxide, and borage oil, with some clinical evidence in particular for silver, though more research is needed.[8] Phototherapy with narrow-band UV-B and UV-A1 has also seen a considerable amount of research and is likely effective for reducing the severity of eczema.[9]
Most individuals with eczema suffer with chronically itchy skin. Topical barrier creams, corticosteroids, and antihistamines are often used initially, but for many these are not sufficient, and additional methods of itch-control are often used before resorting to immunosuppressive drugs. The first step to managing itch is prevention, with the most common being a daily bathing and moisturizing routine using eczema medications. Unfortunately, scratching the affected skin can sometimes make eczema worse — leading to more rashes, thickened skin, and infections.
There are several at-home remedies for itchy skin including:
- Low-pH skin cleansers
- Cold compress
- Pinching and patting the itchy skin instead of scratching
- Acv, baking soda, or oatmeal soap bath
- Wet wrap therapy
- Frequently moisturizing the affected area[15]
We can not currently vouch for the efficacy of these methods, but they are commonly used.
Genetics plays a considerable role, and a number of mechanistically plausible genes have been linked to eczema risk.[10] Additionally, microbiome disruption is highly common in eczema, and with the vital role in immune regulation that the microbiome plays, this is plausible.[11] Other possible factors include smoking, maternal alcohol consumption and stress/anxiety, being born in winter, phthalate exposure, and hard water. The early-life use of antibiotics[12] and acetaminophen are also associated with eczema, though it's possible that this is due to a dysfunctional immune system leading both to the need for those medications as well as eczema.
A family history of atopic diseases — and atopic dermatitis in particular — is the strongest predictor, with twin studies suggesting a very high genetic component.[10] Most of the genetic causes aren’t well understood, but one of the most likely contributors are gene variants of the filaggrin gene (FLG), which codes for filaggrin, an important structural protein of the epidermis that maintains proper skin barrier function.[16][17][18] That said, most people with atopic dermatitis don’t have any FLG mutations, and a majority of people with FLG mutations won’t develop atopic dermatitis, so it’s only one part of the picture. Another genetic cause is gene variants of the serine peptidase inhibitor kazal type 5 (SPINK5) gene, which codes for a protein that helps regulate desquamation (peeling/shedding of the outermost layer of skin, which is a normal part of cell turnover but can go awry), preventing excessive breakdown of the stratum corneum (the outermost layer of skin). It also has implications for the skin barrier and skin dryness.[19]
Besides FLG and SPINK5, some other genes related to atopic dermatitis are also related to immune function and inflammation, namely the cytokines IL-4 and IL-10.[20][21] Gene variants in TLR2 and TLR4, which are involved in the activation of inflammatory signaling, are also associated with a higher risk.[22]
Atopic dermatitis is a multifaceted disease with many processes that work together; variations in genes related to skin cell turnover, skin barrier maintenance, and inflammation are all likely to contribute.
The gut microbiome is involved in the regulation of immune function, with symbiotic bacteria helping to curtail immune activation that can aggravate atopic dermatitis. There is evidence that the gut microbiome is less diverse and there are fewer of some beneficial species in people with atopic dermatitis.[11] Interestingly, dysbiosis in infants is associated with atopic dermatitis later in life.
It’s possible that, instead of alterations in the skin microbiome causing atopic dermatitis, the skin condition leads to microbial changes. Consequently, these changes in the skin microbiome can be seen as more of an exacerbating factor in atopic dermatitis rather than an initial cause, though a causal role is possible in some instances.[23][24] In atopic dermatitis, the lesions are extremely likely to have an overabundance of the bacterium Staphylococcus. aureus, which can worsen inflammation and lead to dysregulated desquamation and insufficient beneficial species. Fungi of the Malassezia genus, as well as some others, may also aggravate atopic dermatitis in some scenarios. There is also the phenomenon of the herpes simplex virus migrating to atopic dermatitis lesions and causing complications, called eczema herpeticum.[24]
Lower microbial diversity and low populations of beneficial species in the gut are associated with the risk for atopic dermatitis. When it comes to the skin microbiome, an imbalance is likely more of a consequence of atopic dermatitis than an initial cause, though a partial role can’t be ruled out in some cases.
Both active smoking and secondhand smoke exposure increase the risk of atopic dermatitis.[25] Smoking has the potential to disrupt the healthy functioning of the immune system, both aggravating pathogenic (potentially disease-causing) immune responses and impairing protective ones.[26] Prenatal exposure to smoking wasn’t associated with atopic dermatitis risk in general but has been in studies conducted in Asia.[27][25] The reason for this discrepancy is unknown.
One meta-analysis found an association between maternal alcohol consumption and atopic dermatitis in offspring.[28] Interestingly, it didn’t find an association between alcohol consumption and the skin condition for adults. It should be noted that these observations are based on a relatively small amount of research. It is possible that alcohol exposure in utero can lead to an immune system imbalance — called Th2 dominance — that is more associated with atopic dermatitis, but there may be other reasons.
There is some evidence that being born in winter or fall is associated with a greater prevalence of atopic dermatitis.[29] One probable reason for this is lower humidity and an increased risk of skin dryness and disrupted skin barrier function during the first months of life. Higher immune activity during winter has also been observed, which could increase the likelihood of excessive skin inflammation. Vitamin D levels are a plausible cause, but the evidence for this scenario specifically isn’t compelling.[30][31]
A meta-analysis found that a mother taking probiotic mixtures during pregnancy or breastfeeding can reduce the risk of atopic dermatitis in her children.[32] This provides evidence that the maternal gut microbiome during pregnancy is relevant to offspring, though evidence outside of the context of probiotic supplementation is lacking. Another meta-analysis, investigating the effects of Lactobacillus and Bifidobacterium bacteria mixtures in children, also found convincing evidence for a reduction in risk.[33] However, it should be noted that almost all studies included supplementation during pregnancy; only two studies didn’t. Yet another study looked at any probiotic supplementation and found notable benefits when women took probiotics during pregnancy. A total of 5 studies looked only at supplementation for infants; the results were positive overall, but we can’t be sure of them, and more research is needed.[34] The evidence for giving infants and children probiotics for prevention is promising but very preliminary.
Early-life antibiotic use is associated with a higher risk of atopic dermatitis, though this could be as a result of an increased risk of infections due to other factors that further increase the risk of the skin condition.[12]
Being overweight or gaining a large amount of weight during pregnancy is associated with a higher risk of atopic dermatitis in children, while low weight gain during pregnancy is associated with a lower risk.[35] These risks are small, and the extent to which the weight gain itself — rather than confounding factors, such as stress — plays a role is unclear.
Preliminary evidence suggests that maternal stress, anxiety, and adverse life events that could be causes of stress and anxiety are associated with a greater risk of atopic dermatitis in their children.[36]
There is also some evidence that prenatal phthalate exposure increases the risk. [37]
The gut microbiome seems to be critical early in life to the risk for atopic dermatitis. Probiotic use during pregnancy and breastfeeding are likely protective, while antibiotic use is associated with a higher risk. Adverse prenatal conditions, such as excessive weight gain, stress and anxiety, or exposure to alcohol or phthalates, are also associated with an increased risk.
References
Examine Database References
- Skin Quality - Callaway J, Schwab U, Harvima I, Halonen P, Mykkänen O, Hyvönen P, Järvinen TEfficacy of dietary hempseed oil in patients with atopic dermatitisJ Dermatolog Treat.(2005 Apr)
- Eczema Symptoms - Lee J, Jung E, Koh J, Kim YS, Park DEffect of rosmarinic acid on atopic dermatitisJ Dermatol.(2008 Dec)
- Eczema Symptoms - Farahani AM, Aryanian Z, Memariani Z, Mozaffarpur SA, Shirafkan HA Comparison of the Effect of Topical Preparation of L. and Hydrocortisone on Hand Eczema: A Double-Blind Randomized Controlled Trial.J Altern Complement Med.(2021-Apr)
- Eczema Symptoms - Bamford JT, Ray S, Musekiwa A, van Gool C, Humphreys R, Ernst EOral evening primrose oil and borage oil for eczema.Cochrane Database Syst Rev.(2013-Apr-30)
- Skin Dryness - Verallo-Rowell VM, Dillague KM, Syah-Tjundawan BSNovel antibacterial and emollient effects of coconut and virgin olive oils in adult atopic dermatitisDermatitis.(2008 Nov-Dec)
- Wound Healing - Gebicki J, Sysa-Jedrzejowska A, Adamus J, Woźniacka A, Rybak M, Zielonka J1-Methylnicotinamide: a potent anti-inflammatory agent of vitamin originPol J Pharmacol.(2003 Jan-Feb)